Aug 31 – Lecture 1 – Introduction
4 Themes
1. Lactation
2. Social Development
3. Piglet Vitality
- immune competence
4. Vitality of Chickens
- Closure / Ethics in animal husbandry
Introduction Adaptive Capacity
“The ability of an animal to adapt to a changing environment with minimum loss of function (Brooks
and Adger, 2005)”
Factors to adapt to:
- Climate
- Housing system
- Pathogens
- Interactions with other animals and man
Environmental demands > adaptive capacity -> risk of dysfunction
Recognition of no adaptation
- Behavioural problems
Tail biting, feather pecking
- Metabolic disorders
Severe negative energy balance cattle and pigs (early lactation -> feed intake not high
enough)
- Health problems
Weaning piglets, ascites in broilers
- Reproductive problems
Broiler breeders, pigs and cattle
How to balance adaptive capacity with environment (selection, development, facilitation)
1. Change the adaptive capacity of an animal by experience and learning
Genetic selection (e.g. natural antibodies -> first line defence/innate (not specific)
immune system (broad affinity to bind antigens))
Epigenic effects (changing via the mother) -> a (stressful) environment influences the
resilience of the offspring
Pre and post-natal (e.g. perinatal flavour learning -> food neophobia / e.g. EST ->
influence post hatch performance chicken)
2. Facilitate adaptive capacity
Resources and opportunity to provide the ‘right’ environment (e.g. preventing a NEB in
cows, no dry period improves EB at onset lactation)
,Sept 1 – Lecture 2 – Introduction to Lactation
Contents
- Short introduction to lactation - Health consequences of a negative
Lactation: function and variation energy balance
Milk synthesis in mammary cells Negative energy balance
Stages of lactation (‘metabolic load’)
Lactation cycle in dairy cows Health consequences of a NEB
(‘metabolic stress’)
What about pigs?
Unique characterization mammals
Lactation Warm blooded
Hair/fur Backbone
Lactation gives a variety of evolutionary benefits to mammals (all very hygienically)
Moisture
Antimicrobials
Nutrients
Promoting immune development (highly species-specific)
Promoting endocrine development (highly species-specific)
Behavioural development (‘bonding’)
Milk synthesis in the mammary epithelial cell
Raw materials are transferred via the blood stream
Proteins
Synthesized in the secretory cell (=mammary epithelial cell)
From amino acids
Lipids
Short-chain fatty acids (C4-C14) are synthesized in the cells
From volatile fatty acids of rumen origin (dairy cow)
Longer chain fatty acids (>= C16) are preformed (originate from diet or body fat)
Lactose
Synthesized in the secretory cell
From glucose (or glucogenic precursors)
Controls the volume of milk secreted (osmotic value!, also minerals and cells are
important for osmotic value, so with mastitis -> cell count increases and lactose
decreases)
Differences in milk composition across species due to:
- Genetic background - Nutrient requirements infants
- Nursing intervals (example: cape fur - Available nutrients for milk synthesis
seal) - Diet composition
- Growth rate infants - Mobilisation of body reserves
- Developmental stage infants
(associated with lactation stage)
, Stages of lactation
Mammogenesis: growth of the mammary gland
Lactogenesis: functional change of the mammary gland so that it can produce milk
I: colostrogenesis (till birth)
II: milk secretion (starts at birth)
Galactopoiesis: maintenance of lactation (longest stage)
- Important factors
Galactopoietic hormones (prolactin, growth hormone (dairy cows))
Removal of (accumulated) milk! (stimulates blood flow / Feedback inhibitor of lactation
(FIL-produced by mammary cells when they produce milk) is present in milk, so milk
inhibits milk production)
Involution: cessation of lactation
- All stages are predominantly controlled by the endocrine system
- All stages are affecting/affected by management/environment
Negative Energy Balance (NEB)
Energy balance = (Energy intake) – (Energy requirements)
For lactating (&pregnant) cows:
Energy balance = (Energy intake) – (Energy for maintenance + milk + pregnancy)
NEB when intake < requirements: body weight loss by mobilising body compositions (74% body fat +
6% body protein + 20% water)
(Body weight change, Body fat thickness & Body condition scores and other methods are used to determine
NEB) (NEB can be split in protein balance and fat balance -> fat balance is far more important for NEB)
Why a NEB in early lactation?
Peripartum feed intake depression (reduce in feed intake before giving birth)
- Don’t want the digestive system to be active at the moment of giving birth
- Calf grows fast and takes in a lot of space (stomach capacity reduces)
- Because of stress -> calving period is stressful -> reduces feed intake
- Leptin is present in body fat and not beneficial for feed intake so fat cows have a higher
reduction in feed intake than cows with less body fat
Health consequences
Successful in evolution = A * B
Where A = number of viable young per unit of time (fertility, milk), B = surviving as long as possible
(health)
Trade-off between A and B when resources are limiting! (and within A or B?)
There is also trade-off between the current calf (‘milk production’) and future calf (‘fertility’)
Most cells in de body need insulin to facilitate glucose uptake, except for the brain, placenta, and the
mammary gland. Low insulin facilitates glucose intake by the mammary gland. So, low insulin inhibits
glucose uptake by other cells and facilitates glucose intake by the mammary gland. Therefore, when
cows are selected on low insulin, a higher milk yield can be obtained (higher priority for milk
production/current calf) (glucose is an essential nutrient for lactose production).
, NEB is associated with diseases and disorders (Lack of adaptation):
Increase in metabolic disorders
Fatty liver
Ketosis
Increase in infectious diseases
Mastitis
Laminitis
Decrease in reproductive performance
Increase in veterinary costs and reduced animal welfare
Laminitis associated with early lactation:
High concentrate intake / low feed intake
more fermentable carbohydrates/less fibre
saliva production & rumination time decreases
ruminal pH decreases (rumen acidosis)
dying of rumen bacteria
endotoxin release in the rumen, which enters the bloodstream
vasodilatation
damage to blood vessels in hoof (because of narrow space -> high pressure)
Mastitis associated with early lactation (cows):
1. Start of lactation (Oliver and Sordillo, 1988)
Open teat canal (hygiene)
Intramammary pressure (oedema) -> milk leakage (nutrient source for bacteria)
Loss of protective effect of preventive antibiotics & presence of environmental pathogens
2. Reduced immune competence (?!!)
“42% of sows are replaced per year (Siva, 2003) of which 54% can be attributed to lactation-
associated problems (D’allaire et al., 1986)”
Periparturient Hypogalactia Syndrome (PHS, Sows) – early lactation
Classification of possible causes, which can lead to PHS:
1. Non – infectious (mammary gland edema, teat malformations)
2. Infectious (e.g. mastitis)
3. Nutrition: feed intake!!! (fat sows have a lower feed intake than non-fat sows)
Overfeeding during gestation (-> reduced feed intake in lactation)
Low energy intake during lactation
Constipation (fiber!)
4. Management & environment
Inadequate ventilation
Poor hygiene
Stress (e.g. change of diet)
4 Themes
1. Lactation
2. Social Development
3. Piglet Vitality
- immune competence
4. Vitality of Chickens
- Closure / Ethics in animal husbandry
Introduction Adaptive Capacity
“The ability of an animal to adapt to a changing environment with minimum loss of function (Brooks
and Adger, 2005)”
Factors to adapt to:
- Climate
- Housing system
- Pathogens
- Interactions with other animals and man
Environmental demands > adaptive capacity -> risk of dysfunction
Recognition of no adaptation
- Behavioural problems
Tail biting, feather pecking
- Metabolic disorders
Severe negative energy balance cattle and pigs (early lactation -> feed intake not high
enough)
- Health problems
Weaning piglets, ascites in broilers
- Reproductive problems
Broiler breeders, pigs and cattle
How to balance adaptive capacity with environment (selection, development, facilitation)
1. Change the adaptive capacity of an animal by experience and learning
Genetic selection (e.g. natural antibodies -> first line defence/innate (not specific)
immune system (broad affinity to bind antigens))
Epigenic effects (changing via the mother) -> a (stressful) environment influences the
resilience of the offspring
Pre and post-natal (e.g. perinatal flavour learning -> food neophobia / e.g. EST ->
influence post hatch performance chicken)
2. Facilitate adaptive capacity
Resources and opportunity to provide the ‘right’ environment (e.g. preventing a NEB in
cows, no dry period improves EB at onset lactation)
,Sept 1 – Lecture 2 – Introduction to Lactation
Contents
- Short introduction to lactation - Health consequences of a negative
Lactation: function and variation energy balance
Milk synthesis in mammary cells Negative energy balance
Stages of lactation (‘metabolic load’)
Lactation cycle in dairy cows Health consequences of a NEB
(‘metabolic stress’)
What about pigs?
Unique characterization mammals
Lactation Warm blooded
Hair/fur Backbone
Lactation gives a variety of evolutionary benefits to mammals (all very hygienically)
Moisture
Antimicrobials
Nutrients
Promoting immune development (highly species-specific)
Promoting endocrine development (highly species-specific)
Behavioural development (‘bonding’)
Milk synthesis in the mammary epithelial cell
Raw materials are transferred via the blood stream
Proteins
Synthesized in the secretory cell (=mammary epithelial cell)
From amino acids
Lipids
Short-chain fatty acids (C4-C14) are synthesized in the cells
From volatile fatty acids of rumen origin (dairy cow)
Longer chain fatty acids (>= C16) are preformed (originate from diet or body fat)
Lactose
Synthesized in the secretory cell
From glucose (or glucogenic precursors)
Controls the volume of milk secreted (osmotic value!, also minerals and cells are
important for osmotic value, so with mastitis -> cell count increases and lactose
decreases)
Differences in milk composition across species due to:
- Genetic background - Nutrient requirements infants
- Nursing intervals (example: cape fur - Available nutrients for milk synthesis
seal) - Diet composition
- Growth rate infants - Mobilisation of body reserves
- Developmental stage infants
(associated with lactation stage)
, Stages of lactation
Mammogenesis: growth of the mammary gland
Lactogenesis: functional change of the mammary gland so that it can produce milk
I: colostrogenesis (till birth)
II: milk secretion (starts at birth)
Galactopoiesis: maintenance of lactation (longest stage)
- Important factors
Galactopoietic hormones (prolactin, growth hormone (dairy cows))
Removal of (accumulated) milk! (stimulates blood flow / Feedback inhibitor of lactation
(FIL-produced by mammary cells when they produce milk) is present in milk, so milk
inhibits milk production)
Involution: cessation of lactation
- All stages are predominantly controlled by the endocrine system
- All stages are affecting/affected by management/environment
Negative Energy Balance (NEB)
Energy balance = (Energy intake) – (Energy requirements)
For lactating (&pregnant) cows:
Energy balance = (Energy intake) – (Energy for maintenance + milk + pregnancy)
NEB when intake < requirements: body weight loss by mobilising body compositions (74% body fat +
6% body protein + 20% water)
(Body weight change, Body fat thickness & Body condition scores and other methods are used to determine
NEB) (NEB can be split in protein balance and fat balance -> fat balance is far more important for NEB)
Why a NEB in early lactation?
Peripartum feed intake depression (reduce in feed intake before giving birth)
- Don’t want the digestive system to be active at the moment of giving birth
- Calf grows fast and takes in a lot of space (stomach capacity reduces)
- Because of stress -> calving period is stressful -> reduces feed intake
- Leptin is present in body fat and not beneficial for feed intake so fat cows have a higher
reduction in feed intake than cows with less body fat
Health consequences
Successful in evolution = A * B
Where A = number of viable young per unit of time (fertility, milk), B = surviving as long as possible
(health)
Trade-off between A and B when resources are limiting! (and within A or B?)
There is also trade-off between the current calf (‘milk production’) and future calf (‘fertility’)
Most cells in de body need insulin to facilitate glucose uptake, except for the brain, placenta, and the
mammary gland. Low insulin facilitates glucose intake by the mammary gland. So, low insulin inhibits
glucose uptake by other cells and facilitates glucose intake by the mammary gland. Therefore, when
cows are selected on low insulin, a higher milk yield can be obtained (higher priority for milk
production/current calf) (glucose is an essential nutrient for lactose production).
, NEB is associated with diseases and disorders (Lack of adaptation):
Increase in metabolic disorders
Fatty liver
Ketosis
Increase in infectious diseases
Mastitis
Laminitis
Decrease in reproductive performance
Increase in veterinary costs and reduced animal welfare
Laminitis associated with early lactation:
High concentrate intake / low feed intake
more fermentable carbohydrates/less fibre
saliva production & rumination time decreases
ruminal pH decreases (rumen acidosis)
dying of rumen bacteria
endotoxin release in the rumen, which enters the bloodstream
vasodilatation
damage to blood vessels in hoof (because of narrow space -> high pressure)
Mastitis associated with early lactation (cows):
1. Start of lactation (Oliver and Sordillo, 1988)
Open teat canal (hygiene)
Intramammary pressure (oedema) -> milk leakage (nutrient source for bacteria)
Loss of protective effect of preventive antibiotics & presence of environmental pathogens
2. Reduced immune competence (?!!)
“42% of sows are replaced per year (Siva, 2003) of which 54% can be attributed to lactation-
associated problems (D’allaire et al., 1986)”
Periparturient Hypogalactia Syndrome (PHS, Sows) – early lactation
Classification of possible causes, which can lead to PHS:
1. Non – infectious (mammary gland edema, teat malformations)
2. Infectious (e.g. mastitis)
3. Nutrition: feed intake!!! (fat sows have a lower feed intake than non-fat sows)
Overfeeding during gestation (-> reduced feed intake in lactation)
Low energy intake during lactation
Constipation (fiber!)
4. Management & environment
Inadequate ventilation
Poor hygiene
Stress (e.g. change of diet)
